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Central IL-1 differentially regulates peripheral IL-6 and TNF synthesis
H Kitamura1, S Okamoto, Y Shimamoto
1Department of Biomedical Sciences, School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
Cellular and Molecular Life Sciences : CMLS
|May 12, 1998
Summary
Central interleukin (IL)-1 triggers autonomic nervous system activation, leading to increased IL-6 production in peripheral organs. This study investigates the brain-body communication pathway for inflammatory responses.
Area of Science:
- Neuroimmunology
- Molecular Biology
- Physiology
Background:
- Central administration of interleukin (IL)-1 is known to induce rapid increases in blood IL-6.
- The precise mechanism underlying this response remains to be fully elucidated.
Purpose of the Study:
- To investigate the effects of intracerebroventricular (i.c.v.) injection of IL-1 beta on IL-6 and tumor necrosis factor (TNF) mRNA expression in rat spleen and liver.
- To explore the role of the autonomic nervous system in mediating these central IL-1-induced responses.
Main Methods:
- Rats received i.c.v. injections of human recombinant IL-1 beta.
- mRNA expression levels of IL-6 and TNF in spleen and liver were measured.
- Chlorisondamine, a ganglionic blocking agent, was used to assess autonomic nervous system involvement.
Main Results:
- I.c.v. IL-1 rapidly increased IL-6 and TNF mRNA levels in both spleen and liver.
- These increases occurred prior to or in parallel with elevated serum levels of these cytokines.
- Chlorisondamine pretreatment significantly inhibited IL-6 responses but had minimal effect on TNF responses.
Conclusions:
- Brain IL-1, acting through the autonomic nervous system, stimulates peripheral IL-6 production.
- The autonomic nervous system does not appear to mediate the peripheral production of TNF induced by central IL-1.
- This highlights a specific neural pathway for IL-6 regulation by central IL-1.